The results showed that HKY could induce apoptosis in colon cancer cell line through downregulation of p-Akt1, Rel A, Bcl-XL, pro-caspase 3, and pro-caspase 9 expressions, and upregulation of BAX, cleaved caspase-3, and cleaved caspase-9.
Selectively blocking FAK-Akt1 interaction by a peptide derived from the FAK-Four-point-one, ezrin, radixin, moesin (FERM) domain reduces colon cancer cell adhesion <i>in vitro</i> and in mice.
The results revealed that resveratrol treatment and AKT1 knockdown significantly inhibited cell migration and invasion in colon cancer, and markedly increased E‑cadherin expression and decreased that of N‑cadherin, phospho (p)‑AKT1, p‑GSK‑3β, and Snail in colon cancer both in vitro and in vivo.
Overexpression or silencing of TUSC3 could partially reverse the effects of the overexpression or repression of miR-873-5p on colon cancer progression caused by activation of the AKT pathway.
Taken together, the present results suggest that the targeting effects of resveratrol to AKT1 and AKT2 may be a potent strategy for chemoprevention or therapy for colon cancer.
In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK‑JNK‑mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti‑cancer agent for colon carcinoma therapy.
These findings demonstrate a heretofore unappreciated, but critical, role for nCDase in enabling/maintaining basal activation of AKT and also suggest that nCDase is a suitable novel target for colon cancer therapy.
The aim of this study was to explore whether LINC00657 can regulate cell proliferation and invasion by regulating the PI3K/AKT pathway and thus participate in the occurrence of colon cancer.
The results of the present study verified that the protective effects of miRNA-29a suppress the PTEN/Akt/GSK3β and Wnt/β-catenin signaling pathways in colon cancer.
In the present study, DLD-1 isogenic AKT1, AKT2 and AKT1/2 knockout colon cancer cell lines were used as a model system in conjunction with the parental cell line in order to further elucidate the differences between the AKT isoforms and how they are involved in various cellular pathways.
Anti-colon cancer activity of Murraya koenigii leaves is due to constituent murrayazoline and O-methylmurrayamine A induced mTOR/AKT downregulation and mitochondrial apoptosis.
INPP4B inhibits PtdIns(3,4)<i>P</i><sub>2</sub>-mediated AKT activation in breast and prostate cancer; however, INPP4B expression is increased in acute myeloid leukaemia (AML), melanoma and colon cancer where it paradoxically promotes cell proliferation, transformation and/or drug resistance.
The aim of the in vitro study was to investigate the anticancer activity of InsP6 on colon cancer with the focus on inhibiting the AKT1 kinase and p70S6K1 as mTOR effector, in relation to proliferation and apoptosis of cells.
The present study demonstrated that upregulation of miR-542-3p inhibited the growth and invasion of colon cancer cells through PI3K/AKT/survivin signaling, highlighting a novel therapeutic approach for the treatment of colon cancer.
Curcumin synergizes with 5-fluorouracil by impairing AMPK/ULK1-dependent autophagy, AKT activity and enhancing apoptosis in colon cancer cells with tumor growth inhibition in xenograft mice.